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Understanding your Mold Air Quality Report


There are over 200 species of fungi to which people are routinely exposed indoors and outdoors (NAS, 2000). These include mold-like fungi, as well as other fungi such as yeasts (unicellular fungi forming pasty colonies) and mushrooms, which are characterized by the familiar fruiting bodies people think of as “mushrooms.” The terms “mold” and “mildew” are non-technical names commonly used to refer to any fungus that is growing in the indoor environment (Burge and Otten, 1999). These names are used interchangeably, although mildew is often applied to growths on fabrics, window sills, or bathroom tiles. Because molds and mildews may be any of several natural classes of fungi, these names are not interchangeable with the nomenclature used in biological classification systems (Burge and Otten, 1999). In general, molds are characterized by a visible vegetative body, or colony, composed of a network (mycelium) of threadlike filaments (hyphae), which infiltrate the mold’s food or habitat. Mold colonies may appear cottony, velvety, granular, or leathery, and maybe white, gray, black, brown, yellow, greenish, or other colors (Burge and Otten, 1999). Many reproduce via the production and dispersion of spores. They are usually saprophytes (i.e., they feed on dead organic matter) and, provided with sufficient moisture, can live off of many materials found in homes, such as wood, cellulose in the paper backing on drywall, insulation, wallpaper, glues used to bond carpet to its backing, and everyday dust and dirt. Research indicates that certain molds can cause a variety of adverse human health effects, including allergic reactions and immune responses (e.g., asthma), infectious disease (e.g., histoplasmosis1 ), and toxic effects (e.g., aflatoxin-induced liver cancer) (ACGIH, 1999). Molds are thought to play a role in asthma in several ways. They are known to produce a large number of proteins that are potentially allergenic, and there is sufficient evidence to support associations between fungal allergen exposure and asthma exacerbation and upper respiratory disease (NAS, 2000). In addition, molds may play a role in asthma via the release of irritants that increase the potential for sensitization, or the release of toxins (mycotoxins) that affect immune response (NAS, 2000). Finally, mold toxins can cause direct lung damage leading to pulmonary diseases other than asthma (NAS, 2000).

Results of skin-prick testing 2 of 1,286 children with asthma in the National Cooperative Inner-City Asthma Study (NCICAS) showed that the most common positive allergen sensitivity in these children was to Alternaria (38%), followed by cockroach (36%), and the Dermatophagoides pteronyssinus house dust mite (31%) (Kattan et al., 1997).

While detecting allergic sensitization to molds is difficult in infants, some data suggest that infants at risk for developing allergic disease experience respiratory symptoms which may or may not be allergic in nature. In a study conducted by Belanger et al. (2003), a positive exposure-response was found between levels of mold (measured by a portable air sampler) in the home and wheeze/persistent cough in the first year of life among children whose mothers had asthma, and between mold levels and persistent cough among children of mothers without asthma. Gent et al. (2002) assessed the potential for the increased incidence of respiratory symptoms after household exposure to particular fungal genera, namely Cladosporium (in 62% of homes) and Penicillium (in 41% of homes) in a population of infants 1-12 months of age at high risk for developing asthma. To the extent that the measured mold sampled represented longer-term exposure concentrations, the study results suggested that the infants studied who were exposed to high levels of Penicillium had higher rates of wheezing and persistent cough. The authors also suggested that because there are considerable seasonal variations in some molds, including Cladosporium, intermittent exposures may contribute only sporadically to respiratory symptoms. Other molds, such as Penicillium, seem to be present at more consistent levels year-round. Previous studies note that relationships between exposure to mold and respiratory symptoms of children are complicated and may depend on a variety of potentially confounding factors, such as the season in which mold samples were collected and the presence of other moisture dependent biological hazards such as endotoxins (Gent et al., 2002; Thorne et al., 2005).


Mold exposure in homes occurs primarily via inhalation of airborne spores and fungal fragments; some airborne fragments have very small particle sizes and may be far more numerous than airborne spores (Green et al., 2005; Gorny et al., 2002). Molds are also present in household dust and on surfaces, with exposure occurring when particles are disturbed and become airborne or, less commonly in residential situations, through dermal contact or ingestion. The release of mold spores or fragments into indoor air from mold colonies is usually dependent on some sort of mechanical disturbance, although for some types of molds slight air movement may be sufficient (e.g., air movement by a fan), or spores may become airborne through natural spore discharge mechanisms. Most molds release spores ranging in size from 2 to 10 µm (although some genera, such as Alternaria, have conidia (a type of spore) ranging from 20-60 µm), but some may be released as chains or clumps of spores (NAS, 2000). Allergens. Many molds produce numerous protein or glycoprotein allergens capable of causing allergic reactions in people. These allergens have been measured in spores, as well as other fungal fragments (Green et al., 2005; Sporik, 1993); however, most allergen seems to be located in germinating spores, in the hyphal tips, and in mycelia (Mitakakis et al., 2001; Green et al., 2003). Some of the major fungal allergens identified and isolated to date include those from Aspergillus fumigatus, Aspergillus oryzae, Alternaria alternata, Cladosporium herbarum, Penicillium citrinum, Penicillium chrysogenum, Trichophyton tonsurans, Malassezia furfur, and Psilocybe cubensis (NAS, 2000). An estimated 6-10% of the general population and 15- 50% of those who are genetically susceptible (atopic) are sensitized to mold allergens (NAS, 2000). Research clearly indicates that exposure to mold plays a role in the exacerbation of asthma symptoms in sensitized individuals, although the association between mold exposure and asthma development remains undetermined (IOM, 2004; NAS, 2000). The clearest association between mold exposure and asthma is for sensitization to Alternaria (Halonen et al., 1997; Perzanowski et al., 1998), although this may be because the allergens of this genus (Alt a 1 and Alt a 2) are well characterized relative to other mold species (Ibarrola et al., 2004; Asturias et al., 2005; NAS, 2000; Platts-Mills and Woodfolk, 2000).